By: Joel Michael Reynolds

During the last week of November, a number of articles appeared with eye-catching titles like, “Scientists Find a Way to Prevent, Reverse Chronic Pain” or “‘Off Switch’ for Pain Discovered in the Brain.” They reported the discovery that by only activating a single receptor, named A3, with small amounts of adenosine molecules, rodents’ chronic pain stopped or even reversed. While the pain relieving effects of adenosine were well known, studies had shown it to cause significant side effects, and this new study was thought to not do so because it tripped only the A3 adenosine receptor pathway. The problem is that we likely won’t enjoy the promises of those sensational headlines, for reports such as these rely upon and contribute to a widespread misunderstanding of the nature of pain—especially chronic pain. The American Academy of Pain Medicine reports that pain affects 100 million people, “more Americans than diabetes, heart disease and cancer combined…A recent market research report indicates that more than 1.5 billion people worldwide suffer from chronic pain” in particular.﻿[1]﻿ But if all we need to stop chronic pain is a simple ‘off switch,’ why have over 40 years of pain research, the creation of thousands of pain research centers across the world, and the medical establishment of pain specialists failed in finding it?[2] The short answer is that pain is not like a light bulb. There is no simple “off switch.” It is less a current or flame, and more a force.Typical, acute pain (like holding one’s hand over a fire) occurs from anticipated or actual nerve damage. Quick acting A-δ nerve fibers lead an organism to move itself away from the localized cause of pain, while the restorative system enlists the slower C fibers to kick in long after the acute occurrence and thus lead one to immobilize the area in order to heal.[3]In cases related to acute pain, clinicians can focus not simply on symptoms, but also on their underlying causes like tissue damage. Yet many chronic pain syndromes, such as CRPS/RSD (Complex Regional Pain Syndrome Type 1, formerly Reflex Sympathetic Dystrophy), seem to occur without nerve or tissue damage. This complexity adds to the puzzling fact that whereas the ability to experience pain is a crucial adaptational tool for human and many non-human organisms, chronic pain is maladaptive. The search for easy fixes to pain relief is old, but science is still in its infancy with respect to understanding pain, especially of the chronic sort.

Neurobiological research, building on the influential gate-theory of pain by Melzack and Wall, has shown pain to adaptively regulate the conscious and unconscious actions of a human organism via complex, intermodal sensory-discriminative and affective-cognitive interactions.[4].We now know that pain is not just a matter of physical sensation; it is an emotional and social phenomenon as well. Qualitative research has shown it to be experienced in significantly different ways along lines of sex, race, age, and class, among other categories.[5]Pain is not simple.As beneficial as the study on A3AR may be, it still relies on a simplistic, symptomatic approach. It does not address the cause of chronic pain. While there is substantial and ongoing research into a variety of symptomatic approaches, from tamper-proof, high-power opioids to spinal simulators, the holy grail of pain research is to understand the cause of chronic pain and develop methods to treat it. Yet, the complexity of chronic pain as a research topic and as a lived experience is lost amidst reports on the sheer number of people with chronic pain or, worse, reports that myopically focus on opioid-abuse, a framing that still lingers from the failed and continually failing Nixon-era war on drugs.[6] The reduction of pain policy to drug policy[7] works in tandem with the unending production of articles about how to reduce, control, or eliminate pain in medical news and media. Pain becomes a problem to be solved by adding or removing some factor. Pop a pill here, outlaw a pill there. Activate a receptor here, deactivate a receptor there. But these approaches reveal a failure to comprehend the phenomenon of pain. Pain, like gravity, is a force. We can measure it, feel it, alter it, study it, and even exploit it, but we still don’t really know how it works. Especially for those whose lives become defined by it, hopefully we someday will.

Joel is a Ph.D. candidate (ABD) in the Department of Philosophy and an Emory Arts & Sciences Graduate Fellow at Emory University. As the current Laney Graduate School Disability Studies Fellow, he is also the program coordinator for theEmory Disability Studies Initiative.